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Infection and Immunity, October 1999, p. 5117-5123, Vol. 67, No. 10
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Differential Transcription of the tcpPH Operon Confers Biotype-Specific Control of the Vibrio cholerae ToxR Virulence Regulon

Yvette M. Murley,1 Patricia A. Carroll,1,dagger Karen Skorupski,2 Ronald K. Taylor,2 and Stephen B. Calderwood1,3,*

Infectious Disease Division, Massachusetts General Hospital, Boston, Massachusetts 021141; Department of Microbiology, Dartmouth Medical School, Hanover, New Hampshire 037552; and Department of Microbiology and Molecular Genetics, Harvard Medical School, Boston, Massachusetts 021153

Received 26 March 1999/Returned for modification 20 May 1999/Accepted 27 July 1999

Epidemic strains of Vibrio cholerae O1 are divided into two biotypes, classical and El Tor. In both biotypes, regulation of virulence gene expression depends on a cascade in which ToxR activates expression of ToxT, and ToxT activates expression of cholera toxin and other virulence genes. In the classical biotype, maximal expression of this ToxR regulon in vitro occurs at 30°C at pH 6.5 (ToxR-inducing conditions), whereas in the El Tor biotype, production of these virulence genes only occurs under very limited conditions and not in response to temperature and pH; this difference between biotypes is mediated at the level of toxT transcription. In the classical biotype, two other proteins, TcpP and TcpH, are needed for maximal toxT transcription. Transcription of tcpPH in the classical biotype is regulated by pH and temperature independently of ToxR or ToxT, suggesting that TcpP and TcpH couple environmental signals to transcription of toxT. In this study, we show a near absence of tcpPH message in the El Tor biotype under ToxR-inducing conditions of temperature and pH. However, once expressed, El Tor TcpP and TcpH appear to be as effective as classical TcpP and TcpH in activating toxT transcription. These results suggest that differences in regulation of virulence gene expression between the biotypes of V. cholerae primarily result from differences in expression of tcpPH message in response to environmental signals. We present an updated model for control of the ToxR virulence regulon in V. cholerae.

* Corresponding author. Mailing address: Infectious Disease Division, Massachusetts General Hospital, 55 Fruit St., Boston, MA 02114. Phone: (617) 726-3811. Fax: (617) 726-7416. E-mail: scalderwood{at}partners.org.

dagger Present address: Scriptgen Pharmaceuticals, Inc., Waltham, MA 02154.

Infection and Immunity, October 1999, p. 5117-5123, Vol. 67, No. 10
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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